增强胸腺功能作为COVID-19的替代治疗方案

M. Genebat, A. Calderón, L. Tarancón-Díez, M. Muñoz-Fernández, M. Leal
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引用次数: 2

摘要

由SARS-CoV-2感染(COVID-19疾病)引起的大流行已在全球范围内扩大。目前,除了其他合并症外,高龄是死亡率和严重临床结局的独立预测因子[1]。可以解释老年受试者严重临床结果的潜在分子和细胞机制尚不清楚[2],尽管已有研究表明免疫衰老和低水平全身性炎症(炎症老化)也可能起相关作用[3,4]。如今,除了开发有效的疫苗外,研究工作还集中在治疗方法上,以最大限度地减少病毒复制和进一步的炎症级联反应,从而导致呼吸窘迫和多器官衰竭;然而,到目前为止,尚未建立针对SARS-CoV-2感染的特异性治疗方法[5]。目前用于sars - cov -2感染受试者的抗病毒和免疫调节药物基于其作用机制或体外疗效的生物学合理性,尚未获得明确的科学证据,有待于前瞻性临床试验的明确和结结性结果。总而言之,需要关于导致COVID-19疾病临床结果受损的潜在机制的替代假设。从这个意义上说,即使是普遍接受的细胞因子风暴的作用也受到了质疑[6]。因此,更大的假设被认为是更大和更有益的治疗方案可以测试。最近,我们小组提出胸腺功能障碍可能在老年sars - cov -2感染受试者的临床预后受损中发挥相关作用[7]。因此,本文的主要目的是在增强胸腺功能的基础上探索一种新的COVID-19疾病治疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Enhanced Thymopoiesis as an Alternative Therapeutic Option for COVID-19
The pandemic caused by SARS-CoV-2 infection (COVID-19 disease) has expanded worldwide. Currently, it is well known that advanced age is an independent predictor of mortality and severe clinical outcome, apart from other comorbidities [1]. Underlying molecular and cellular mechanisms that could explain the severe clinical outcome among elderly subjects are not well known [2], although it has been described that both immunosenescence and a low-level systemic inflammation (inflamm-aging) could also play a relevant role [3,4]. Now a days, apart from an effective vaccine development, research efforts are focused on therapeutic approaches that could minimize both the viral replication and the further inflammatory cascade driving to respiratory distress and multiorgan failure; however, up to now, no specific therapy for SARS-CoV-2 infection has been established [5]. Awaiting for definitive and conclusive results from prospective clinical trials, antiviral and immunomodulatory drugs currently employed in SARS-CoV-2-infected subjects are based on their biological plausibility according to the mechanism of action or in vitro efficacy, but not in a definitive scientific evidences. Taken altogether, alternative hypothesis about underlying mechanisms driving to an impaired clinical outcome in COVID-19 disease are required. In this sense, even the universally accepted role of the cytokine storm has been questioned [6]. Hence, the greater hypothesis is considered the greater and more beneficial therapeutic options could be tested. Recently, our group has suggested that thymic dysfunction could play a relevant role in the impaired clinical outcome observed in elderly SARS-CoV-2-infected subjects [7]. Thus, the main objective of the present opinion paper is to explore a new therapeutic option for COVID-19 disease, based on enhancing thymic function.
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